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CRT & RRT Exam Secrets Study Guide

"How to Ace the Certified Respiratory Therapist (CRT) Exam and Registered Respiratory Therapist (RRT) Exam, using our easy step-by-step CRT & RRT test study guide, without weeks and months of endless studying..." Morrison Media

 

 

 

 

1. Patients with high plateau airway pressures (> 35 cm)  

  1. Causes:

    • Excessively high tidal volume

    • Pneumothorax or massive pleural effusion

    • Microatelectasis (due to ARDS, etc.)

    • Cardiogenic pulmonary edema

    • Secretions or foreign body in the airway

    • Kinking or obstruction of the endotracheal tube or ventilator tubing

    • Ascites or abdominal distension

    • Bronchospasm

    • Severe intrinsic lung disease (pulmonary fibrosis, etc.)

    • Patient "fighting" the ventilator

 

  1. Treatment:

    • Insure that the patient is optimally suctioned and that all bronchospasm is being treated.  When giving bronchodilators by MDI to ventilated patients, more puffs should be given - generally 4 puffs of albuterol; attention should be given to the manner that MDIs are introduced into the ventilator circuit since directing the MDI spray toward the wall of the ventilator tubing drastically reduces the delivered dose (Fink, 1996)

    • Check a chest x-ray to insure that there is no pneumothorax

    • Treat the underlying cause of stiff lungs (diuresis for pulmonary edema, antibiotics for diffuse pneumonia, etc.)

    • Insure that total body oxygen requirements are maximally reduced:

a)     treat fever

b)     sedate patients who are moving a great deal

c)     treat infection 

·         Optimize oxygen delivery

a)     transfuse patients with severe anemia (the optimal hemoglobin in acute respiratory failure has not been determined and probably depends on the individual patient but pending definitive studies, a useful rule is to keep the hemoglobin > 9 gm)

·         Add PEEP to the "best PEEP" level to optimally open otherwise closed alveoli during expiration and therefore reduce the pressure required to open these alveoli during inspiration

·         Reduce peak inspiratory flow rate

a)     this will effectively increase inspiratory time and decrease expiratory time

b)     in its extreme, it results in "inverse ratio ventilation" with an I:E ratio < 1:1 (a normal ventilated patient has an I:E ratio of about 1:2 or 1:3)

·         Reduce tidal volume

(a)  if the respiratory rate is unchanged, this can result in so called "controlled hypoventilation" when the minute ventilation is allowed to decrease below the patient's natural minute ventilation (by either a decrease in the tidal volume or a decrease in the respiratory rate); this can result in an increase in pCO2 ("permissive hypercapnia") and usually requires the patient to be heavily sedated since hypercapnia can be quite uncomfortable

(b)  the lowest tolerable pH during controlled hypoventilation is unclear but pending definitive studies, it is probably desirable to keep the pH > 7.20 during hypoventilation

·         Sedation and/or paralysis (see below)

·         Change to pressure control ventilation mode 

 

2.      Patients with persistent hypoxemia despite FiO2 > 50%  

  1. Causes:

    • Underlying intrinsic lung disease (pneumonia, pulmonary edema, etc.)

    • Central airway obstruction (bronchospasm, secretions, foreign body, neoplasm, etc.)

    • Intra cardiac shunt (especially patent foramen ovale)

    • Pulmonary embolus

    • Other pulmonary vascular disease (pulmonary hypertension, etc.)

    • AutoPEEP

 

  1. treatment:

·         Suction the airways to remove secretions, etc.

·         Administer bronchodilators if indicated

·         Therapeutic bronchoscopy if there is evidence of atelectasis or lobar collapse

·         Add PEEP to the optimal level

·         Diagnose and treat underlying causes (above), especially pulmonary embolus

·         Transfuse to keep hemoglobin > 9 gm to insure sufficient oxygen delivery despite low PO2

·         In patients with severe ARDS or alveolar hemorrhage, consider placing the patient in the prone position as this can improve oxygenation by up to 15% in these situations (Chatte, 1997)

 

3.      Patients with autoPEEP  

  1. Causes:

·         Fundamentally, this is the pressure associated with an end-expiratory volume which is higher than the normal functional residual capacity (FRC)

a)     this is most commonly seen in patients with obstructive airways disease in whom there is insufficient time for full exhalation resulting in "air trapping" and associated progressive hyperinflation

b)     it can also occur in persons without obstructive airways disease who have insufficient time for normal exhalation (eg, hyperventilation or too high of a tidal volume) 

·         AutoPEEP should be suspected when:

a)     any patient with obstructive airways disease is receiving mechanical ventilation

b)     any patient with unexplained hypotension after initiating mechanical ventilation

c)     any patient with unexplained tachycardia after initiating mechanical ventilation 

·         AutoPEEP can be inferred by any of three findings:

a)     an expired air volume that is less than the inspired volume (trapped air)

b)     a flow-time graphic (available on many newer ventilators) showing that flow never reaches 0 before the next breath (in other words, the patient is still expiring when the next breath is delivered)

c)     chest auscultation demonstrating that expiratory noises (wheezing, etc.) are audible all the way up until the next breath is delivered 

·         Cannot be measured directly from the ventilator dials

a)     autoPEEP represents the pressure in the alveoli and not the pressure in the ventilator circuit; therefore, there can be life-threatening autoPEEP despite an end-expiratory pressure of 0 on the ventilator pressure meter (Leatherman, 1996)

b)     the expiratory port of the ventilator circuit must be occluded in order to allow the pressure within the airway to equilibrate and register on the pressure dial 

 

  1. Treatment:

    • Reduce tidal volume

    • Increase peak inspiratory flow (allowing more expiratory time)

    • Reduce respiratory rate

    • Sedate the hyperventilating patient

    • Permit controlled hypoventilation (see below)

    • Treat any bronchospasm

    • Consider switching to pressure support mode

 

4.      Patients with ARDS   

·         A low tidal volume strategy of 6 ml/kg was associated with a 22% improvement in mortality (31% vs. 39%) and a greater number of ventilator-free days in the first 4 weeks of hospitalization (12 vs. 10) compared to a traditional/high tidal volume ventilation strategy of 12 ml/kg. There was also less multiple organ system failure and lower blood interleukin-6 levels in the low tidal volume group (ARDS network, N Engl J Med 2000)

·         Pressure control ventilation can be useful on occasion

·         PEEP needs to be judiciously adjusted and can result in substantially improved oxygenation

·         Prone ventilation can result in improved oxygenation

 

 

 

 

 
 

    

       

 

 

 

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